Inferior wall myocardial infarctions responsible for recognition of right ventricular infarction with heart failure.
Increased awareness of right ventricular infarction alone or with left ventricular infarction underlines the importance of the right ventricle.
Growing interest in non-invasive recognition of right ventricular infarction due to therapeutic implications in distinguishing from left ventricular dysfunction.
Right ventricular infarctions with inferior infarctions have higher hypotension, bradycardia, mortality compared to isolated infarctions.
Right ventricular infarction causes when blood supply to right ventricle is acutely interrupted from artery blockage.
RV blood supply is mainly from RCA including the proximal segment, which also supplies SA and AV nodes. Ischemia and damage in the RV decrease its ability to pump blood and left ventricular preload.
Epidemiology
Rare isolated right ventricular infarction seen with inferior wall myocardial infarction. Incidence of right ventricular infarction ranges from 10% to 50%.
Clinically evident right ventricular infarction is rare in living subjects compared to autopsy findings due to diagnostic challenges.
Transient right ventricular dysfunction and stunning complicate accurate estimation of infarction incidence.
Criteria for diagnosing right ventricular infarction may underestimate its true incidence despite strict adherence.
Anatomy
Pathophysiology
Perfusion occurs in cardiac cycle during systole and diastole with increased oxygen extraction under stress.
Right coronary artery supplies inferior wall of right ventricle, acute marginal branches supply anterior wall, and conus branch supplies infundibulum of right ventricle.
Prompt reperfusion of blocked coronary artery linked to right ventricular infarction lowers right atrial pressure. Severity of infarction depends on site of occlusion in right ventricular arterial supply.
Proximity of right coronary artery occlusion to infarction site directly relates to size of right ventricular infarction in research studies.
Etiology
The causes of RVI are:
Coronary artery dissection
Right ventricular strain from pulmonary hypertension
Right coronary artery occlusion
Embolism
Genetics
Prognostic Factors
RV dysfunction severity impacts prognosis. Extensive RV infarcts result in poor outcomes, increased hemodynamic compromise, and higher risk of heart failure.
RVIs accompany LV inferior wall heart attacks. Poorer outcomes result if both ventricles are affected due to hypotension/cardiac output.
RVIs and inferior wall myocardial infarctions with LV involvement have worse prognosis due to combined ventricular dysfunction causes hypotension.
RVI near SA and AV nodes can cause bradycardia, heart block, and conduction issues including complete heart block.
Clinical History
Collect details including symptoms, medication, and family history to understand clinical history of patient.
Physical Examination
Peripheral Examination
Abdominal Examination
Cardiac Auscultation
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Symptoms are hypotension, bradycardia, jugular venous distension, right-sided heart failure, and cardiogenic shock.
Differential Diagnoses
Cor Pulmonale
Pneumothorax Imaging
Endomyocardial Fibrosis
Hypertrophic Cardiomyopathy
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Consider right ventricular infarction in inferior MI patients with hypotension and no rales.
Left ventricular dysfunction may require balloon pump or nitroprusside infusion
Patients categorized with presence of right ventricular failure or cardiogenic shock in study.
Patients with right ventricular dysfunction and shock need adequate right-sided filling pressures and left ventricular preload.
Consider inotropic therapy for right ventricular failure alongside optimized end-diastolic pressure.
Evidence shows early presentation within 6 hours of inferior infarction onset benefits right ventricular involvement.
The main procedural intervention is percutaneous coronary intervention including thrombolytic therapy, temporary pacing, mechanical circulatory support, and pericardiocentesis may be needed based on the patient’s hemodynamic status.
The initial treatment phase includes immediate stabilization, symptom relief, and revascularization.
Pharmacologic therapy is effective in the treatment phase as it includes inotropic agents, tissue plasminogen activators, adrenergic agonists, and antidiuretic hormone analogs.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and intervention therapies.
The regular follow-up visits with the cardiologist are scheduled to check the improvement of patients along with treatment response.
Inferior wall myocardial infarctions responsible for recognition of right ventricular infarction with heart failure.
Increased awareness of right ventricular infarction alone or with left ventricular infarction underlines the importance of the right ventricle.
Growing interest in non-invasive recognition of right ventricular infarction due to therapeutic implications in distinguishing from left ventricular dysfunction.
Right ventricular infarctions with inferior infarctions have higher hypotension, bradycardia, mortality compared to isolated infarctions.
Right ventricular infarction causes when blood supply to right ventricle is acutely interrupted from artery blockage.
RV blood supply is mainly from RCA including the proximal segment, which also supplies SA and AV nodes. Ischemia and damage in the RV decrease its ability to pump blood and left ventricular preload.
Rare isolated right ventricular infarction seen with inferior wall myocardial infarction. Incidence of right ventricular infarction ranges from 10% to 50%.
Clinically evident right ventricular infarction is rare in living subjects compared to autopsy findings due to diagnostic challenges.
Transient right ventricular dysfunction and stunning complicate accurate estimation of infarction incidence.
Criteria for diagnosing right ventricular infarction may underestimate its true incidence despite strict adherence.
Perfusion occurs in cardiac cycle during systole and diastole with increased oxygen extraction under stress.
Right coronary artery supplies inferior wall of right ventricle, acute marginal branches supply anterior wall, and conus branch supplies infundibulum of right ventricle.
Prompt reperfusion of blocked coronary artery linked to right ventricular infarction lowers right atrial pressure. Severity of infarction depends on site of occlusion in right ventricular arterial supply.
Proximity of right coronary artery occlusion to infarction site directly relates to size of right ventricular infarction in research studies.
The causes of RVI are:
Coronary artery dissection
Right ventricular strain from pulmonary hypertension
Right coronary artery occlusion
Embolism
RV dysfunction severity impacts prognosis. Extensive RV infarcts result in poor outcomes, increased hemodynamic compromise, and higher risk of heart failure.
RVIs accompany LV inferior wall heart attacks. Poorer outcomes result if both ventricles are affected due to hypotension/cardiac output.
RVIs and inferior wall myocardial infarctions with LV involvement have worse prognosis due to combined ventricular dysfunction causes hypotension.
RVI near SA and AV nodes can cause bradycardia, heart block, and conduction issues including complete heart block.
Collect details including symptoms, medication, and family history to understand clinical history of patient.
Peripheral Examination
Abdominal Examination
Cardiac Auscultation
Symptoms are hypotension, bradycardia, jugular venous distension, right-sided heart failure, and cardiogenic shock.
Cor Pulmonale
Pneumothorax Imaging
Endomyocardial Fibrosis
Hypertrophic Cardiomyopathy
Consider right ventricular infarction in inferior MI patients with hypotension and no rales.
Left ventricular dysfunction may require balloon pump or nitroprusside infusion
Patients categorized with presence of right ventricular failure or cardiogenic shock in study.
Patients with right ventricular dysfunction and shock need adequate right-sided filling pressures and left ventricular preload.
Consider inotropic therapy for right ventricular failure alongside optimized end-diastolic pressure.
Evidence shows early presentation within 6 hours of inferior infarction onset benefits right ventricular involvement.
Cardiology, General
Reduce noise in hospital to prevent excessive stimulation of the autonomic nervous system.
Avoid high fowler’s position to prevent reduced venous return and increased thoracic pressure.
Provide blankets to ensure ambient temperature can prevent unnecessary strain on the heart.
Proper awareness about right ventricular infarction should be provided and its related causes with management strategies.
Appointments with a cardiologist and preventing recurrence of disorder is an ongoing life-long effort.
Cardiology, General
Dobutamine:
It produces vasodilation to increase the inotropic state.
Milrinone:
It inhibits phosphodiesterase type III in cardiac and smooth vascular muscle.
Cardiology, General
Reteplase:
It forms plasmin to facilitate cleavage of endogenous plasminogen.
Norepinephrine:
It increased afterload to decrease cardiac output.
Cardiology, General
Vasopressin:
It promotes smooth muscle contraction through the vascular bed of the renal tubular epithelium.
Cardiology, General
The main procedural intervention is percutaneous coronary intervention including thrombolytic therapy, temporary pacing, mechanical circulatory support, and pericardiocentesis may be needed based on the patient’s hemodynamic status.
Cardiology, General
The initial treatment phase includes immediate stabilization, symptom relief, and revascularization.
Pharmacologic therapy is effective in the treatment phase as it includes inotropic agents, tissue plasminogen activators, adrenergic agonists, and antidiuretic hormone analogs.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and intervention therapies.
The regular follow-up visits with the cardiologist are scheduled to check the improvement of patients along with treatment response.
Inferior wall myocardial infarctions responsible for recognition of right ventricular infarction with heart failure.
Increased awareness of right ventricular infarction alone or with left ventricular infarction underlines the importance of the right ventricle.
Growing interest in non-invasive recognition of right ventricular infarction due to therapeutic implications in distinguishing from left ventricular dysfunction.
Right ventricular infarctions with inferior infarctions have higher hypotension, bradycardia, mortality compared to isolated infarctions.
Right ventricular infarction causes when blood supply to right ventricle is acutely interrupted from artery blockage.
RV blood supply is mainly from RCA including the proximal segment, which also supplies SA and AV nodes. Ischemia and damage in the RV decrease its ability to pump blood and left ventricular preload.
Rare isolated right ventricular infarction seen with inferior wall myocardial infarction. Incidence of right ventricular infarction ranges from 10% to 50%.
Clinically evident right ventricular infarction is rare in living subjects compared to autopsy findings due to diagnostic challenges.
Transient right ventricular dysfunction and stunning complicate accurate estimation of infarction incidence.
Criteria for diagnosing right ventricular infarction may underestimate its true incidence despite strict adherence.
Perfusion occurs in cardiac cycle during systole and diastole with increased oxygen extraction under stress.
Right coronary artery supplies inferior wall of right ventricle, acute marginal branches supply anterior wall, and conus branch supplies infundibulum of right ventricle.
Prompt reperfusion of blocked coronary artery linked to right ventricular infarction lowers right atrial pressure. Severity of infarction depends on site of occlusion in right ventricular arterial supply.
Proximity of right coronary artery occlusion to infarction site directly relates to size of right ventricular infarction in research studies.
The causes of RVI are:
Coronary artery dissection
Right ventricular strain from pulmonary hypertension
Right coronary artery occlusion
Embolism
RV dysfunction severity impacts prognosis. Extensive RV infarcts result in poor outcomes, increased hemodynamic compromise, and higher risk of heart failure.
RVIs accompany LV inferior wall heart attacks. Poorer outcomes result if both ventricles are affected due to hypotension/cardiac output.
RVIs and inferior wall myocardial infarctions with LV involvement have worse prognosis due to combined ventricular dysfunction causes hypotension.
RVI near SA and AV nodes can cause bradycardia, heart block, and conduction issues including complete heart block.
Collect details including symptoms, medication, and family history to understand clinical history of patient.
Peripheral Examination
Abdominal Examination
Cardiac Auscultation
Symptoms are hypotension, bradycardia, jugular venous distension, right-sided heart failure, and cardiogenic shock.
Cor Pulmonale
Pneumothorax Imaging
Endomyocardial Fibrosis
Hypertrophic Cardiomyopathy
Consider right ventricular infarction in inferior MI patients with hypotension and no rales.
Left ventricular dysfunction may require balloon pump or nitroprusside infusion
Patients categorized with presence of right ventricular failure or cardiogenic shock in study.
Patients with right ventricular dysfunction and shock need adequate right-sided filling pressures and left ventricular preload.
Consider inotropic therapy for right ventricular failure alongside optimized end-diastolic pressure.
Evidence shows early presentation within 6 hours of inferior infarction onset benefits right ventricular involvement.
Cardiology, General
Reduce noise in hospital to prevent excessive stimulation of the autonomic nervous system.
Avoid high fowler’s position to prevent reduced venous return and increased thoracic pressure.
Provide blankets to ensure ambient temperature can prevent unnecessary strain on the heart.
Proper awareness about right ventricular infarction should be provided and its related causes with management strategies.
Appointments with a cardiologist and preventing recurrence of disorder is an ongoing life-long effort.
Cardiology, General
Dobutamine:
It produces vasodilation to increase the inotropic state.
Milrinone:
It inhibits phosphodiesterase type III in cardiac and smooth vascular muscle.
Cardiology, General
Reteplase:
It forms plasmin to facilitate cleavage of endogenous plasminogen.
Norepinephrine:
It increased afterload to decrease cardiac output.
Cardiology, General
Vasopressin:
It promotes smooth muscle contraction through the vascular bed of the renal tubular epithelium.
Cardiology, General
The main procedural intervention is percutaneous coronary intervention including thrombolytic therapy, temporary pacing, mechanical circulatory support, and pericardiocentesis may be needed based on the patient’s hemodynamic status.
Cardiology, General
The initial treatment phase includes immediate stabilization, symptom relief, and revascularization.
Pharmacologic therapy is effective in the treatment phase as it includes inotropic agents, tissue plasminogen activators, adrenergic agonists, and antidiuretic hormone analogs.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and intervention therapies.
The regular follow-up visits with the cardiologist are scheduled to check the improvement of patients along with treatment response.
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